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Ssri Withdrawal Hypoglycemia

Many Psychiatric Symptoms Remit Upon Drug Withdrawal – Even Suicidal Impulses

Many Psychiatric Symptoms Remit Upon Drug Withdrawal – Even Suicidal Impulses

This is something I’ve posted before that bears repeating. It was written while I was still withdrawing off the final of the six drugs I came off of. I completed the psychiatric drug withdrawal a little over a year ago (it’s been 6 years as of 2016). I made some comments to bring it up to date upon reposting all written in this blue font. And for anyone dealing with suicidal feelings, whether on or off psych drugs see: Suicide prevention: alternative ways to approach folkss **warning — rapid or cold-turkey withdrawal can often inflame psychiatric symptoms (including feelings of hurting oneself) for some time. For safer withdrawal practices see here. Something that comes up quite often in discussions with my friends and readers who have been on meds and have come off of them is how many of the “psychiatric” symptoms they were being “treated” for disappear upon discontinuation of the medications. This is widely known and experienced among those of us who have decided to stop medicating ourselves. For me there are two most astonishing details. The first was when I discovered I was being given more and more Risperdal to medicate away the akathisia that the Risperdal was causing! Once off the Risperdal the akathisia was gone and so was most of what we’d called anxiety which led me to take massive doses of benzos. This is tragic and disgusting. I often have had considerably less anxiety in the midst of an awful withdrawal then I had when I was on the six drugs. I’m on one drug now and withdrawal from benzos is infamous for causing horrible rebound anxiety and yet it’s not terribly true for me. (this has changed the closer to zero I’ve gotten, though it seems to be a physiological response particularly to withdrawal from what I can gather in withdrawal ci Continue reading >>

Neonatal Adaptation In Infants Prenatally Exposed To Antidepressants- Clinical Monitoring Using Neonatal Abstinence Score

Neonatal Adaptation In Infants Prenatally Exposed To Antidepressants- Clinical Monitoring Using Neonatal Abstinence Score

Abstract Intrauterine exposure to antidepressants may lead to neonatal symptoms from the central nervous system, respiratory system and gastrointestinal system. Finnegan score (Neonatal Abstinence Score, NAS) has routinely been used to assess infants exposed to antidepressants in utero. Retrospective cohort study of women using antidepressants during pregnancy and their infants. Patients were identified from the electronic health record system at Karolinska University Hospital Huddinge containing pre-, peri- and postnatal information. Information was collected on maternal and infant health, social factors and pregnancy. NAS sheets were scrutinized. Results 220 women with reported 3rd trimester exposure to SSRIs or SNRIs and who gave birth between January 2007 and June 2009 were included. Seventy seven women (35%) used citalopram, 76 used (35%) sertraline, 34 (15%) fluoxetine and 33 (15%) other SSRI/SNRI. Twenty-nine infants (13%) were admitted to the neonatal ward, 19 were born prematurely. NAS was analyzed in 205 patients. Severe abstinence was defined as eight points or higher on at least two occasions (on a scale with maximum 40 points), mild abstinence as 4 points or higher on at least two occasions. Seven infants expressed signs of severe abstinence and 46 (22%) had mild abstinence symptoms. Hypoglycemia (plasma glucose <2.6 mmol/L) was found in 42 infants (19%). Severe abstinence in infants prenatally exposed to antidepressants was found to be rare (3%) in this study population, a slightly lower prevalence than reported in previous studies. Neonatal hypoglycemia in infants prenatally exposed to antidepressant may however be more common than previously described. Figures Citation: Forsberg L, Navér L, Gustafsson LL, Wide K (2014) Neonatal Adaptation in Infants Pre Continue reading >>

Neonatal Adverse Events Associated With In Utero Ssri/snri Exposure

Neonatal Adverse Events Associated With In Utero Ssri/snri Exposure

Objectives 1. Highlight language in SSRI/SNRI class labeling a) PRECAUTIONS- Pregnancy non-teratogenic section b) DOSAGE and ADMINISTRATION section 2. Provide rationale for proposing class labeling Terms Used for Neonatal SSRI/SNRI Syndromes - SRI Withdrawal - SRI Toxicity - Poor Neonatal Adaptation - Serotonergic Excess - Serotonergic CNS Adverse Effects - Serotonin Syndrome SSRI/SNRI Discontinuation Symptoms in Adults1 Dysequilibrium: dizziness, vertigo, ataxia GI: nausea, vomiting Flu-like: fatigue, lethargy, myalgia, chills Sensory disturbance: paresthesia, electric shock sensation Sleep disturbance: insomnia, vivid disturbing dreams Neuropsychiatric symptoms 1Schatzberg AF, et al. Serotonin reuptake inhibitor discontinuation syndrome: A hypothetical definition. J Clin Psychiatry 1997; 58 [suppl 7] 5-10. Similarities Between Neonatal AE & Adult Discontinuation Symptoms Neonatal “Withdrawal†Irritability, jitteriness, agitation, insomnia, poor feeding, crying AE onset: 10 to 36 hours Resolution: 1 to 14 days Adult Withdrawal Irritability, anxiety, agitation, insomnia, anorexia, GI distress AE onset: 24 to 72 hours Resolution: 1 to 14 days Similarities Between Neonatal AE & Toxicity in Adults Neonatal “Toxicity†Jitteriness, insomnia, hypertonia, myoclonus, hyperreflexia, convulsions, temperature dysregulation, autonomic instability, tachypnea Onset: immediate to several hours Resolution: hours to weeks May have high serum SSRI/SNRI levels Adult Toxicity Jitteriness, insomnia, hypertonia, myoclonus, hyperreflexia, akathisia, convulsions, temperature dysregulation, autonomic instability, tachypnea, cognitive symptoms Onset: highly variable Resolution: hours to several days May have high serum SSRI/SNRI levels Rationale for Proposing Class Labeling N Continue reading >>

Hypoglycemia - A Hidden Hell

Hypoglycemia - A Hidden Hell

~ S P E C I A L ~ F E A T U R E ~ by Connie Bennett, M.S.J., C.H.H.C. an excerpt from the new book SUGAR SHOCK! How Sweets and Simple Carbs Can Derail Your Life -- And How You Can Get Back on Track by Connie Bennett, M.S.J., C.H.H.C. with Stephen T. Sinatra, M.D. Foreword by Nicholas Perricone, M.D. Published by Berkley Books Reprinted with Permission "Spills the beans on the shocking impact of simple carbohydrates on aging and quality of life..." -- Frequent Oprah Winfrey guest Mehmet C. Oz, M.D., coauthor, YOU: On A Diet INTRODUCTION This excerpt (from Chapter 13) tells the sad story of how millions of Americans are plagued by a mysterious constellation of symptoms but don't know what's wrong with them -- and often, neither do their doctors. Unfortunately, the physicians and loved ones of these ailing millions often wrongly assume that they're "hypochondriacs" or that they have a mental disorder. Worse yet, they think these symptoms are indicative of another disease or condition. Instead, these suffering millions may be victims of SUGAR SHOCK! They're suffering from reactive hypoglycemia, a condition that's often maligned and dismissed by members of the mainstream medical establishment. But cutting-edge nutritionists and medical practitioners contend that hypoglycemia (low blood sugar) is rampant today and usually triggered by excessively consuming sweets or processed carbohydrates -- something most Americans do. Tragically, people who suffer from hypoglycemia are often misdiagnosed for years -- and even frequently advised to seek psychiatric counseling and/or take psychiatric drugs. But usually the best treatment for hypoglycemia is quite simple: Just kick all sugars and processed, "culprit carbs," and eat modest amounts of nourishing, wholesome foods five or six tim Continue reading >>

Mao Inhibitors: The Forgotten Antidepressant That Saved My Life

Mao Inhibitors: The Forgotten Antidepressant That Saved My Life

A science writer recounts his longtime struggle with panic disorder, which led to an unusual solution I had my first panic attack in 1972 when I was 20 years old and a student at the University of London. It took me 10 years to be diagnosed and another 15 years to find a medication that would help me. The medication is Nardil (phenelzine) and it is a monoamine oxidase inhibitor or MAOI, the oldest antidepressant. The drug is rarely used anymore and most people, including young doctors and medical students, don't know much about it. If you've heard the term MAOI, it is probably in conjunction with an ad for a drug such as Prozac (fluoxetine) and the warning "don't take this drug if you are on an MAO inhibitor." Nardil has saved me from a life of fear, shame, loneliness and isolation. It allows me to write, have relationships, play tennis and travel – things I could not do when my panic attacks were at their worst. Hardly anyone takes MAO inhibitors anymore because they have dietary restrictions and interactions with other drugs and because of the popularity of selective serotonin reuptake inhibitors, or SSRIs, antidepressants which can also be effective treatments for panic disorder. This class of drugs includes Prozac (fluoxetine) Zoloft (sertraline) Lexapro (escitalopram) and Paxil (paroxetine). However, Prozac, the first SSRI, was not approved for use until 1987 by the US Food and Drug Administration (FDA). So even if I had been diagnosed properly in 1972, these drugs were not an option. I also had the misfortune of developing panic attacks before panic disorder was recognized as a distinct illness. In the late 1970s, researchers had seen enough cases like mine to realize they were dealing with an illness that did not fit the pattern of traditional anxiety. People h Continue reading >>

Hypoglycemia May Occur With Prozac

Hypoglycemia May Occur With Prozac

I recently spoke with a friend with diabetes who had just started Prozac. He was amazed to find he was having repeated hypoglycemia within days after starting the drug, and had to cut back on his insulin doses. He obviously wondered if it were somehow due to Prozac. Prozac has been a wonder drug for the treatment of depression, but it has a possible effect on diabetes that has not been widely recognized. Prozac, a brand name for the drug fluoxetine, was introduced in the 1980’s, and was the first in a class of antidepressant medications called SSRIs (selective serotonin reuptake inhibitors). It turns out that Prozac (and other SSRIs) have a possible effect of concern for people with diabetes: they can lower blood glucose enough to require downward adjustment of medications taken for control of diabetes. I went to the drug’s label, as posted at the FDA website. The possibility of hypoglycemia when on Prozac has been in the Prozac label for years. It currently reads: “Glycemic Control - In patients with diabetes, PROZAC may alter glycemic control. Hypoglycemia has occurred during therapy with PROZAC, and hyperglycemia has developed following discontinuation of the drug. As is true with many other types of medication when taken concurrently by patients with diabetes, insulin and/or oral hypoglycemic, dosage may need to be adjusted when therapy with PROZAC is instituted or discontinued.” That’s exactly the same wording as the earliest label I can find on-line, from 1999. And if you go to Prozac’s website, it’s right there on the first page: “People who have diabetes and take PROZAC may have problems with low blood sugar while taking PROZAC. High blood sugar can happen when PROZAC is stopped. Your healthcare provider may need to change the dose of your diabet Continue reading >>

Antidepressant Medication As A Risk Factor For Type 2 Diabetes And Impaired Glucose Regulation

Antidepressant Medication As A Risk Factor For Type 2 Diabetes And Impaired Glucose Regulation

OBJECTIVE Antidepressant use has risen sharply over recent years. Recent concerns that antidepressants may adversely affect glucose metabolism require investigation. Our aim was to assess the risk of type 2 diabetes associated with antidepressants through a systematic review. RESEARCH DESIGN AND METHODS Data sources were MEDLINE, Embase, PsycINFO, The Cochrane Library, Web of Science, meeting abstracts of the European Association for the Study of Diabetes, American Diabetes Association, and Diabetes UK, Current Controlled Trials, ClinicalTrials.gov, U.K. Clinical Research Network, scrutiny of bibliographies of retrieved articles, and contact with relevant experts. Relevant studies of antidepressant effects were included. Key outcomes were diabetes incidence and change in blood glucose (fasting and random). RESULTS Three systemic reviews and 22 studies met the inclusion criteria. Research designs included 1 case series and 21 observational studies comprising 4 cross-sectional, 5 case-control, and 12 cohort studies. There was evidence that antidepressant use is associated with type 2 diabetes. Causality is not established, but rather, the picture is confused, with some antidepressants linked to worsening glucose control, particularly with higher doses and longer duration, others linked with improved control, and yet more with mixed results. The more recent, larger studies, however, suggest a modest effect. Study quality was variable. CONCLUSIONS Although evidence exists that antidepressant use may be an independent risk factor for type 2 diabetes, long-term prospective studies of the effects of individual antidepressants rather than class effects are required. Heightened alertness to potential risks is necessary until these are complete. Antidepressant medication use has Continue reading >>

Herbe Aux Mille Vertus

Herbe Aux Mille Vertus

Amber, Amber Touch-and-Heal, Barbe de Saint-Jean, Chasse-diable, Demon Chaser, Fuga Daemonum, Goatweed, Hardhay, Herbe à la Brûlure, Herbe à Mille Trous, Herbe Aux Fées, Herbe Aux Mille Vertus, Herbe Aux Piqûres, Herbe de Saint Éloi, Herbe de la Saint-Jean, Herbe du Charpentier, Herbe Percée, Hierba de San Juan, Hypereikon, Hyperici Herba, Hypericum, Klamath Weed, Klamathaweed, Millepertuis, Millepertuis Perforé, Perforate St. John's Wort, Racecourse Weed, Rosin Rose, Saynt Johannes Wort, SJW, Tipton Weed. CAUTION: See separate listing for Succinate (Amber). Orally, St. John's wort is used for depression, dysthymia, heart palpitations, mood disturbances and other symptoms of menopause, somatization disorder, premenstrual syndrome (PMS), attention deficit-hyperactivity disorder (ADHD), social phobia, obsessive-compulsive disorder (OCD), and seasonal affective disorder (SAD). Other uses include smoking cessation, fibromyalgia, chronic fatigue syndrome (CFS), burning mouth syndrome, headache, migraine headache, muscle pain, neuralgia, polyneuropathy, sciatica, and angioplasty. It is also used orally for secondary symptoms associated with depression such as fatigue, loss of appetite, insomnia, and anxiety. It is also used orally for cancer, glioma, vitiligo, herpes simplex, HIV/AIDS, hepatitis C, weight loss, as a diuretic, and for irritable bowel syndrome (IBS). Oily St. John's wort preparations are used orally for gastric indigestion. Topically, oily St. John's wort preparations are used for treating bruises and abrasions, inflammation and muscle pain, plaque psoriasis, first degree burns, wound healing, tooth extraction, bug bites, hemorrhoids, vitiligo, and neuralgia. In manufacturing, the hypericin-free extracts of St. John's wort are used in the making of alco Continue reading >>

Episode 172: Should Ssris And Snris Be Discontinued In The Setting Of Active Bleeding?

Episode 172: Should Ssris And Snris Be Discontinued In The Setting Of Active Bleeding?

In this episode, I’ll discuss whether selective serotonin reuptake inhibitors (SSRIs) and serotonin norepinephrine reuptake inhibitors (SNRIs) should be discontinued in the setting of active bleeding. I am excited to announce that I have teamed up with the Wegman’s School of Pharmacy St. John Fisher College to offer ACPE Continuing Education credit for listeners of The Elective Rotation podcast! Starting with the February 2017 episodes, I have bundled them into a 1 hour ACPE CE program. You can register by clicking here. If enough participants register, I will publish additional CE programs based on other podcast episodes. Shout out to “Pharmacy Jen” for suggesting this episode topic. Serotonin is often thought of in the context of depression and as a neurotransmitter. However, serotonin and serotonin receptors are present throughout the body in myocardium, blood vessels, GI tract, platelets, smooth muscle, and elsewhere. There are 7 different classes of serotonin receptors, 5-HT1 through 5-HT7. Many receptor classes have several subtypes. Medications are classified as active against specific serotonin receptors based on relative ability to affect a receptor. Remember the irritable bowel syndrome treatment tegaserod? Tegaserod is a serotonin 5-HT4 receptor agonist. While tegaserod had marginal effects on irritable bowel syndrome, it had significant effects on GI motility and the treatment of diabetic gastroparesis. It was being used off label frequently in diabetic patients for pro-motility effects. Unfortunately, the 5-HT4 receptor is also present in myocardium. Tegaserod was soon found to have elevated risk of myocardial infarction and was withdrawn from the market. It is now available only under a special access program. This example serves as a powerful remi Continue reading >>

Infants And Antidepressant Withdrawal

Infants And Antidepressant Withdrawal

Feb. 6, 2006 -- There is growing evidence that babies born to mothers who take antidepressants during pregnancy often experience symptoms of drug withdrawal shortly after birth. In a new study from Israel, about one out of three newborn infants exposed to antidepressants in the womb showed signs of neonatal drug withdrawal, which included high-pitched crying, tremors, and disturbed sleep. Researchers concluded that expectant moms who take selective serotonin reuptake inhibitor (SSRI) antidepressants and their doctors should be warned about the potential risk. "Because maternal depression during pregnancy also entails a risk to the newborn, the risk-benefit ratio of continuing SSRI treatment should be assessed," Rachel Levinson-Castiel, MD, and colleagues wrote. The report comes less than a week after the publication of a major study finding that pregnant women who stop taking antidepressants run a high risk of relapsing into depression. And it comes just months after the FDA warned that a widely prescribed SSRI may be associated with an increased risk of birth defects in babies born to mothers who take the drug in their first trimester. The mixed messages from the research have left many pregnant women who suffer from depression wondering what to do. Diana Dell, MD, who is both an ob-gyn and a psychiatrist, says it is increasingly clear that abruptly stopping depression treatment carries significant risks for both mother and baby. Dell is an assistant professor of obstetrics and gynecology and psychiatry at Duke University in Durham, N.C. "Moms need to be well during pregnancy, and moderate to severe depression certainly has an impact on a developing fetus," she tells WebMD. "We also know that a woman's chance of being hospitalized for psychiatric reasons is greater dur Continue reading >>

Antidepressants Cause 40,000 Deaths A Year - But They're Handed Out Like Candy

Antidepressants Cause 40,000 Deaths A Year - But They're Handed Out Like Candy

My recent article on the dangers of psychiatric drugs ignited a firestorm of controversy. Part of the outrage may have been caused by some general misunderstandings, which I hope to clear up here. This is particularly important at this time as it is abundantly clear that suicide rates rise as the economy worsens. The image of people jumping from windows after the stock market crash of 1929 graphically illustrates this risk. Many may not agree, but I have been studying the economy for over 30 years now and it seems crystal clear to me that the economy has yet to hit bottom, and this will only serve to increase the risk of depression. My Personal Experiences with Depression First of all, I would like to set the record straight as many were confused about my personal experiences with depression. They believed I had none, and therefore there is no way I could understand this disease. Well let me tell you, nothing could be further from the truth. Mental and emotional problems exact an extreme toll on family units and in some cases extended circles of friends. I've personally been a witness to the struggles of two people near and dear to me who suffered from deep chronic depression for a number of years that actually resulted in multiple suicide attempts. Suicide is a common complication of depression, and is one of the primary reasons why it must be taken seriously as it can become a terminal illness. Many also might be unaware that I was a full-time practicing physician for over 20 years before I determined that I could help more people by committing myself full time to this newsletter and web site, than treating patients one on one. Before making that choice however, I treated tens of thousands of people for all sorts of problems, and I've seen my fair share of depressed p Continue reading >>

Adrenal Fatigue

Adrenal Fatigue

The body is uniquely designed to react to any danger or challenge. When it detects the need for 'flight-or-fight,’ the adrenal glands produce a cocktail of hormones that cause the muscles to tense and the heart rate to increase while blood is diverted from the digestive and other organs. After the event, the body and mind relax and harmony is restored. The adrenal glands are involved in multiple functions of the body: stress control metabolism blood sugar and cravings digestion and elimination thyroid reproductive hormones mood and chemical imbalances blood pressure and heart health immune system (allergies, infections, etc.) liver and detoxification centers The adrenal glands are primarily known for the production of our stress hormones Cortisol and Adrenaline, but they are literally a hormone factory that significantly affects the function of every tissue, organ and gland. They produce our anti-aging hormone DHEA, our reproductive hormones: Estrogen, Progesterone and Testosterone, as well as Aldosterone, a hormone that controls the sodium and potassium levels (electrolytes) in the body. If potassium levels become too high, aldosterone is secreted causing the kidneys to excrete more potassium and retain more sodium. Low sodium can also stimulate the secretion of aldosterone. A diet chronically high in potassium or low in sodium can stress the adrenals. Excess potassium is also a natural diuretic and causes some loss of sodium. There should be a balance between potassium and sodium. Please see your physician for an electrolyte blood test to establish your levels. The problem occurs when we are constantly in the 'flight or fight' mode and the adrenals produce too much Cortisol and Adrenaline. When this state of emergency is maintained for extended periods of time, the Continue reading >>

Transient Neonatal Jitteriness Due To Maternal Use Of Sertraline (zoloft®)

Transient Neonatal Jitteriness Due To Maternal Use Of Sertraline (zoloft®)

We describe the occurrence of marked jitteriness and an enhanced startle response in a term infant after being exposed to sertraline in utero. An umbilical cord blood sample taken at the time of birth showed a sertraline concentration (<10 ng/mL) below the reference range. On the third day during the peak of the symptoms, sertraline plasma concentration was <10 ng/mL, while his serotonin level (6 ng/mL) was below the reference range. The neurologic symptoms resolved by the fifth day. To date, there are no reports of transient neonatal jitteriness with maternal use of sertraline documented with low cord and neonatal plasma samples consistent with withdrawal syndrome. Pregnant women are at an increased risk for depression. The prevalence of depression during pregnancy is between 10 and 20%.1,2 Its treatment poses a challenge to clinicians since it requires maximizing maternal treatment while minimizing fetal and neonatal adverse reactions. Selective serotonin reuptake inhibitors (SSRIs) are one class of antidepressants being prescribed for depression during pregnancy. There are published reports suggesting increased neonatal intensive care (NICU) admissions from poor adaptation of newborns exposed to these medications in utero.3 We report the occurrence of marked jitteriness and an enhanced startle response in a term infant after being exposed to sertraline throughout pregnancy documented with cord and neonatal plasma levels. A 4505-g male infant was born at 38 weeks gestation to a 30-year-old gravida 2 para 1 woman with good prenatal care. She was rubella immune and both her gonococcal and chlamydia tests were negative. Her serologic screens were negative for VDRL, HBs Ag, and HIV. She denied smoking, alcoholic beverages and illicit drugs. Her diabetic screen was negativ Continue reading >>

The Selective Serotonin Reuptake Inhibitor Sertraline Enhances Counterregulatory Responses To Hypoglycemia

The Selective Serotonin Reuptake Inhibitor Sertraline Enhances Counterregulatory Responses To Hypoglycemia

Go to: Selective serotonin reuptake inhibitors (SSRIs) are widely prescribed for patients with comorbid diabetes and depression. Clinical case studies in diabetic patients, however, suggest that SSRI therapy may exacerbate hypoglycemia. We hypothesized that SSRIs might increase the risk of hypoglycemia by impairing hormonal counterregulatory responses (CRR). We evaluated the effect of the SSRI sertraline on hormonal CRR to single or recurrent hypoglycemia in nondiabetic rats. Since there are time-dependent effects of SSRIs on serotonin neurotransmission that correspond with therapeutic action, we evaluated the effect of 6- or 20-day sertraline treatment on hypoglycemia CRR. We found that 6-day sertraline (SERT) treatment specifically enhanced the epinephrine response to a single bout of hypoglycemia vs. vehicle (VEH)-treated rats (t = 120: VEH, 2,573 ± 448 vs. SERT, 4,202 ± 545 pg/ml, P < 0.05). In response to recurrent hypoglycemia, VEH-treated rats exhibited the expected impairment in epinephrine secretion (t = 60: 678 ± 73 pg/ml) vs. VEH-treated rats experiencing first-time hypoglycemia (t = 60: 2,081 ± 436 pg/ml, P < 0.01). SERT treatment prevented the impaired epinephrine response in recurrent hypoglycemic rats (t = 60: 1,794 ± 276 pgl/ml). In 20-day SERT-treated rats, epinephrine, norepinephrine, and glucagon CRR were all significantly elevated above VEH-treated controls in response to hypoglycemia. Similarly to 6-day SERT treatment, 20-day SERT treatment rescued the impaired epinephrine response in recurrent hypoglycemic rats. Our data demonstrate that neither 6- nor 20-day sertraline treatment impaired hormonal CRR to hypoglycemia in nondiabetic rats. Instead, sertraline treatment resulted in an enhancement of hypoglycemia CRR and prevented the impaired adr Continue reading >>

Antidepressant Discontinuation: The Why & How Of Tapering

Antidepressant Discontinuation: The Why & How Of Tapering

Note: The author acknowledges, with great compassion, that this is a challenging topic for the many individuals who make the difficult decision to begin treatment with psychiatric medication. All patients must be given the most complete and accurate information about these medications, including: side effects (risk for dependence, violence, impulsivity, etc), the importance of properly tapering off medication, the institutional incentives for medical doctors, educators, and others to advocate for their use, and the availability of effective non-pharmaceutical avenues of treatment that can address root causes of mental illness and behavioral problems. What follows herein is a discussion of steps that the author believes should be taken in anticipation of any medication taper; the subsequent taper should be handled by an experienced professional. Despite these considerations, some patients may be unable to taper which, in the author’s opinion, speaks to the importance of true informed consent prior to medication initiation. This blog is not medical advice and does not replace consultation with a qualified medical professional of your choosing. If you squeeze a spring and you hold it there steadily, for a couple of hours, and then you suddenly let go, what happens? It bursts into expansion, maybe double its natural size and reverberates for a while until it comes to a resting place. This is the example that I use when I describe the effects that antidepressants have on brain chemistry over time – they squeeze the spring and if you let it go too quickly, it’s mayhem. Despite being taught in my training that antidepressants were to the depressed (and to the anxious, OCD, IBS, PTSD, bulemic, anorexic, etc.) what glasses are to the near-sighted, I don’t buy this thinki Continue reading >>

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